The central venous pressure (CVP) refers to the mean vena cava or right atrial pressure, which is equivalent to right ventricular end-diastolic pressure in the absence of tricuspid stenosis. The higher the CVP, the greater the passive diastolic filling of the right ventricle. Per Starling's cardiac function curves in normal hearts, greater filling of the right ventricle leads to a larger right ventricular stroke volume on the subsequent beat. CVP is expressed in millimeters of mercury (mm Hg) or centimeters of water (cm H2O) above atmospheric pressure (1.36 cm H2O=1.0 mm Hg). In most patients, the mean right atrial pressure measured by the CVP closely resembles the mean left atrial pressure (LAP). At the end of diastole, left atrial pressure is assumed to equal left ventricular end diastolic pressure (LVEDP), which in turn is assumed to reflect left ventricular end diastolic volume (LVEDV). Thus, CVP reflects left ventricular preload, a critical parameter in optimizing cardiac function. However, in patients with obstruction, or valvular problems or pulmonary disease the right and left ventricles may function independently. In these less common cases, left ventricular preload should be estimated by measuring the pulmonary capillary ‘wedge’ pressure, using a pulmonary artery catheter (PAC), as this is a better guide to the venous return to the left side of the heart than CVP.
Central venous pressure (CVP) measurement is essential for monitoring hemodynamics in critically ill patients, individuals with heart failure, and patients undergoing surgery to estimate cardiac preload and circulating blood volume. The current standard technique for measurement of CVP is invasive, requiring insertion of a catheter into a subclavian or internal jugular vein, with potential complications. As CVP is the pressure at the right atrium, the system must be “zero-ed” relative to the location of the right atrium or the phlebostatic axis. This reference point is located at the intersection of the fourth intercostal space and mid-axillary line, allowing the measurement to be as close to the right atrium as possible.
CVP can be estimated by physical examination of the jugular veins of the neck. The external jugular vein runs over the sternomastoid muscle and the internal jugular vein runs deep to it. With the subject in a semi-supine position, the lower part of the external jugular vein is normally distended while the upper part is collapsed. Thus, jugular venous pressure (JVP) provides an indirect measure of central venous pressure. The internal jugular vein connects to the right atrium without any intervening valves, acting as a column for the blood in the right atrium. Unfortunately, JVP measurements are difficult and measurement prone due to variance in patient position and clinician measurement techniques. A 1996 systematic review by Cook et al concluded that agreement between doctors on the jugular venous pressure can be poor. Cook, Deborah J., and David L. Simel. “Does this patient have abnormal central venous pressure?.” Jama 275.8 (1996): 630-634. When determining CVP in a heart failure patient by JVP examination, there is the mistaken belief that jugular pulsations are easier to see if the patient is in fluid overload. However, because jugular pulsations depend on right atrial and ventricular contraction, if the patient is in heart failure with a low ejection fraction, the pulsations may be difficult to perceive.
A simple, accurate, noninvasive, and self-administered determination of CVP would represent a valuable tool in the assessment of cardiac function and overall hemodynamic status to include volume status, fluid overload, and left ventricular end diastolic pressure (LVEDP). Such a self-administered test would have significant value in the ambulatory monitoring of the patent with congestive heart failure.
Heart failure occurs due to inadequate cardiac output. Management goals are thus focused on the optimization of stroke volume for the patient with limited cardiac function. Stroke volume is critically dependent on the volume of blood in the left ventricle at the end of diastole, the end diastolic volume. FIG. 1 is a graphical representation of heart performance of a patient with heart failure. The overall performance of the heart in a patient with heart failure is defined by decreased stroke volume when the end diastolic filling pressure exceeds an optimal level. Optimal performance of the heart occurs over a limited range of end diastolic pressures and is labeled “target volume” in the figure and is represented using Frank-Starling curve. Thus, fluid management in these patients is critical; too little fluid leads to decreases stroke volume while fluid overload also leads to decreased stroke volume.
Heart failure is a significant medical problem with an estimated US cost of approximately $30 billion annually with 80% of that expenditure being attributable to hospital admissions. The ability to reduce hospital admissions by improved ambulatory management has been a long-standing clinical objective. The primary cause of heart failure-related hospitalizations is fluid overload. Historical monitoring methods for fluid overload, such as shortness of breath, swelling, fatigue, and weight gain, are not sensitive enough to reflect early pathophysiologic changes that increase the risk of decompensation and subsequent admission to the hospital. Lewin J, Ledwidge M, O'Loughlin C, McNally C, McDonald K. Clinical deterioration in established heart failure: what is the value of BNP and weight gain in aiding diagnosis? Eur J Heart Fail. 2005; 7(6):953-957. Stevenson L, Perloff J K. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989; 261(6):884-888. FIG. 2 shows a typical clinical course of a heart failure patient with increasing fluid overload resulting in hospitalization. Examination of the figure shows that clinically observable signs occur late in the overall decompensation sequence. Thus, the use of clinical symptoms for the management of heart failure patients is problematic.
The difficulty of determining early hemodynamic congestion is demonstrated by the recently completed Better Effectiveness After Transition-Heart Failure (BEAT-HF) study. The study involving more than 1400 patients who were extensively monitored with existing noninvasive technology. The study investigated aggressive management of heart failure patients using a protocol that included pre-discharge heart-failure education, regularly scheduled telephone coaching, and telemonitoring. Telemonitoring included a BLUETOOTH enabled weight scale and blood-pressure/heart-rate monitor integrated with a text device that sent the information to a centralized call center for review (BLUETOOTH is a wireless technology standard used for exchanging data between fixed and mobile devices over short distances using short-wavelength UHF radio waves in the industrial, scientific and medical radio bands, from 2.400 to 2.485 GHz). If predetermined thresholds were exceeded, the patient was called and medication changed as determined by the clinical staff. Also, if significant symptoms were reported, the patient's heart-failure physician was notified and the patient was sent to the emergency department, if necessary. The conclusion from this extensive clinical study was that the intervention had no significant effect on hospital readmission rates.
Decreases in hospital admission rates have been demonstrated by using an invasive-implanted pulmonary artery pressure monitoring system. The CARDIOMEMS HF System measures and monitors the pulmonary artery (PA) pressure and heart rate in heart failure patients. The System consists of an implantable PA sensor, delivery system, and Patient Electronics System. The implantable sensor is permanently placed in the pulmonary artery, the blood vessel that moves blood from the heart to the lungs. The sensor is implanted during a right heart catheterization procedure. The Patient Electronics System includes the electronics unit and antenna. The Patient Electronics System wirelessly reads the PA pressure measurements from the sensor and then transmits the information to the doctor. After analyzing the information, the doctor may make medication changes to help treat the patient's heart failure. In a clinical study in which 550 participants had the device implanted, there was a clinically and statistically significant reduction in heart failure-related hospitalizations for the participants whose doctors had access to PA pressure data. The system costs approximately $2,000 to implant and has a list price of $18,000.
An accurate, self-administered, and noninvasive measurement of CVP would be a significant medical advancement as it would provide information of comparable value to the expensive, invasive CARDIOMEMS system. Specifically, CVP is a measure of right atrial pressure and closely resembles the mean left atrial pressure (LAP). At end diastole left atrial pressure is assumed to equal left ventricular end diastolic pressure (LVEDP), which in turn is assumed to reflect left ventricular end diastolic volume (LVEDV). Thus, CVP is directly related to left ventricular preload, a key parameter in optimizing cardiac output in the heart failure patient.